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To the Editor: Michelson et al1 recently reported differences in platelet glycoprotein IIb/IIIa function in relation to the common PlA1,A2 polymorphism. PlA2-positive platelets showed a lower threshold for activation. This was supported by the gene dosage effect: P1A2 homozygotes had the highest activation of their platelets using a range of ADP concentrations.We are concerned about the conclusions regarding the antiplatelet effects of aspirin reached by the authors. At a low concentration of epinephrine (0.4 μmol/L), there was no difference in platelet aggregation between the PlA1,A1 and PlA1,A2 genotypes, whereas increased aggregation was observed in the PlA2,A2 group. Unexpectedly, the inhibitory effect of aspirin on epinephrine-induced (2.0 μmol/L) platelet aggregation was found in the PlA1,A2 group, but the opposite was found in PlA2,A2 subjects. Two facts could explain this inconsistency. First, in experiments on the platelet aggregation response to aspirin, the number of PlA1,A2 subjects included in the final analysis was diminished by 35%, because 7 of the 20 subjects did not achieve >60% aggregation at 10.0 μmol/L epinephrine. Because platelet response to aspirin was calculated as a percent of aggregation determined in the absence of the inhibitor, the exclusion of “weak responders” could be the cause of a relevant bias. We wonder whether …

Platelet Glycoprotein IIIa Pl A Polymorphism and Effects of Aspirin on Thrombin Generation

Platelet Glycoprotein IIIa Pl ^A Polymorphism and Effects of Aspirin on Thrombin Generation